2020
DOI: 10.1016/j.phrs.2020.105186
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The neuroplasticity marker PSA-NCAM: Insights into new therapeutic avenues for promoting neuroregeneration

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Cited by 14 publications
(8 citation statements)
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“…In a recent report, this molecule is important in the maturation process of mouse cortical immature neurons since the removal of PSA accelerates the final development of these cells [126]. Most importantly, since PSA-NCAM is considered to be a potential target to facilitate repair/regeneration after CNS injury and disease [129], its expression/modulation should be investigated in studies asking whether the immature neurons can be activated in experimental conditions and disease models.…”
Section: Open Questions and Future Perspectivesmentioning
confidence: 99%
“…In a recent report, this molecule is important in the maturation process of mouse cortical immature neurons since the removal of PSA accelerates the final development of these cells [126]. Most importantly, since PSA-NCAM is considered to be a potential target to facilitate repair/regeneration after CNS injury and disease [129], its expression/modulation should be investigated in studies asking whether the immature neurons can be activated in experimental conditions and disease models.…”
Section: Open Questions and Future Perspectivesmentioning
confidence: 99%
“…Three main isoforms have been identified; two are transmembrane forms NCAM-140 and NCAM-180, while the third, NCAM-120 is anchored to the cell membrane through glycosylphosphatidylinositol (GPI) linkage ( Cox et al, 2009 ). Additionally, there is the polysialylated form of the neural cell adhesion molecule called PSA-NCAM; it is well documented that during CNS development, the PSA-NCAM is involved in precursor migration and in neuronal differentiation ( Hu et al, 1996 ; Petridis et al, 2004 ; Bonfanti, 2006 ; Rutishauser, 2008 ; Schuster et al, 2020 ), and also in the regulation of synaptic plasticity in adult brain ( Seki and Arai, 1993 ; Muller et al, 2000 ; Saini et al, 2020 ).…”
Section: Neural Cell Adhesion Molecule: Structure and Functionmentioning
confidence: 99%
“…First, interference with the expression and/or function of these molecules in knock-out mice models or pharmacologically by the administration of antibodies, peptides, enzymes, or antisense oligonucleotides results in impaired long term potentiation (LTP) (Cremer et al, 2000;Eckhardt et al, 2000;Duncan et al, 2021) and learning and memory deficits (Cremer et al, 1994;Arami et al, 1996;Becker et al, 1996;Cambon et al, 2003;Seymour et al, 2008;Bisaz et al, 2009). Second, the converse evidence, i.e., improved LTP and enhanced learning abilities, has been achieved by mimicking NCAM function (Cambon et al, 2004) or by L1 or PSA-NCAM over-expression (Wolfer et al, 1998;Rendeiro et al, 2014;Saini et al, 2020). Third, mRNA and protein expression of NCAM, PSA-NCAM, and L1 in different Abbreviations: NCAM, neural cell adhesion molecule; LTP, long term potentiation; CS, conditioned stimulus; US, unconditioned stimulus; PSA, polysialic acid; EMG, electromyographic; OO, orbicularis oculi; CR, conditioned response; Ipsi, ipsilateral; Contra, contralateral. brain areas is regulated by learning and LTP (Ronn et al, 2000;Hartz and Rønn, 2010;Saini et al, 2020;Duncan et al, 2021).…”
Section: Introductionmentioning
confidence: 99%
“…Second, the converse evidence, i.e., improved LTP and enhanced learning abilities, has been achieved by mimicking NCAM function (Cambon et al, 2004) or by L1 or PSA-NCAM over-expression (Wolfer et al, 1998;Rendeiro et al, 2014;Saini et al, 2020). Third, mRNA and protein expression of NCAM, PSA-NCAM, and L1 in different Abbreviations: NCAM, neural cell adhesion molecule; LTP, long term potentiation; CS, conditioned stimulus; US, unconditioned stimulus; PSA, polysialic acid; EMG, electromyographic; OO, orbicularis oculi; CR, conditioned response; Ipsi, ipsilateral; Contra, contralateral. brain areas is regulated by learning and LTP (Ronn et al, 2000;Hartz and Rønn, 2010;Saini et al, 2020;Duncan et al, 2021). Specifically, the expression of these CAMs is modulated in the hippocampus 1-24 h after LTP induction, by training in a memory task (Fazeli et al, 1994;Schuster et al, 1998;Ronn et al, 2000), or after a variety of hippocampaldependent training experiences including passive avoidance training (Doyle et al, 1992a;Fox et al, 1995Fox et al, , 2000Brandewiede et al, 2014), contextual fear conditioning (Merino et al, 2000;Sandi et al, 2003;Maćkowiak et al, 2009), and olfactory (Knafo et al, 2005a,b), and spatial (Sandi, 2004;Venero et al, 2006;Yamagishi et al, 2018) learning tests.…”
Section: Introductionmentioning
confidence: 99%
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